| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0004069 | L-aspartate:2-oxoglutarate aminotransferase activity | Increases phenotype | PMID:27853831 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:16434500; PMID:37046073 |
| GO:0008219 | Cell death | Increases phenotype | PMID:16239165 |
| GO:0008283 | Cell population proliferation | Affects phenotype | PMID:10951269; PMID:11162775; PMID:11162775; PMID:23626729; PMID:16434500; PMID:23626729; PMID:29626562; PMID:38734220; PMID:9348444 |
| GO:0015908 | Fatty acid transport | Increases phenotype | PMID:28903485 |
| GO:0019395 | Fatty acid oxidation | Increases phenotype | PMID:28903485 |
| GO:0031323 | Regulation of cellular metabolic process | Affects phenotype | PMID:28965233 |
| GO:0031398 | Positive regulation of protein ubiquitination | Increases phenotype | PMID:25285770 |
| GO:0032436 | Positive regulation of proteasomal ubiquitin-dependent protein catabolic process | Decreases phenotype | PMID:25285770 |
| GO:0032930 | Positive regulation of superoxide anion generation | Increases phenotype | PMID:25285770 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:39067772 |
| GO:0045793 | Positive regulation of cell size | Increases phenotype | PMID:28049043 |
| GO:0045795 | Positive regulation of cell volume | Increases phenotype | PMID:38734220 |
| GO:0045834 | Positive regulation of lipid metabolic process | Increases phenotype | PMID:36805544 |
| GO:0051092 | Positive regulation of nf-kappab transcription factor activity | Increases phenotype | PMID:25285770 |
| GO:0051881 | Regulation of mitochondrial membrane potential | Affects phenotype | PMID:37046073 |
| GO:0140042 | Lipid droplet formation | Increases phenotype | PMID:37046073 |
| GO:1903428 | Positive regulation of reactive oxygen species biosynthetic process | Affects phenotype | PMID:26168851 |
We have built a comprehensive resource which compiles potential endocrine disrupting chemicals (EDCs) based on the observed adverse effects or endocrine-mediated endpoints in published experiments on humans or rodents to support basic research. We are not responsible for any errors or omissions in the published research articles or supporting literature on potential EDCs compiled in this resource. Users are advised to exercise their own judgement on the weight of evidence for potential EDCs compiled in this resource. Importantly, our sole goal to build this resource on potential EDCs is to enable future basic research towards better understanding of the systems-level perturbations upon chemical exposure rather than influencing regulatory advice on chemical use.